Renal diseases of acute and chronic nature are widespread in man. Examples of renal diseases are glomerulonephritis, interstitial nephritis, pyelonephritis, glomerulosclerosis, e.g. Kimmelstiel-Wilson in diabetic patients, and post-kidney transplant immune rejection. These diseases are caused by autoimmune processes, various drugs, bacterial invasion or degenerative lesions, respectively. The treatment of renal diseases depends on the causes, e.g. bacterial invasion is treated by application of antibiotics, or, another example, post-kidney-transplant immune rejection is treated by immunosuppression (glucocorticoids, cyclosporin A, etc.). Diminished glomerular filtration and renal plasma flow may be caused by all above mentioned mechanisms and as such could not be treated up to now. Whenever possible, treatment of above mentioned renal diseases consists in the elimination of the causes of the above mentioned pathogenic mechanisms. Consequences of the diminished glomerular filtration and renal plasma flow are the increased blood levels of nitrogene containing metabolites, such as creatinine, urea and uric acid, of pharmaca and their metabolites, as well as of kations and anions of mineral or organic salts. Some of these metabolites and ions are toxic and a surplus thereof may be the reason of certain diseases or at least unpleasant effects.
The major drawbacks of the present methods for the treatment of such toxic effects are that in the case of advanced renal disease they are mostly ineffective. So fare there are no drugs available that improve glomerular filtration and renal plasma flow. There is a definitive need to overcome these drawbacks.
Surprisingly IGF I was now found to improve glomerular filtration and renal plasma flow, in particular also over a prolonged period of time. Advantageously the salt and water balance of the whole body remains constant during treatment with IGF I. No salt or water retention, as seen with growth hormones was observed with IGF I.
IGF I has recently been shown to lower blood glucose in man after intravenous bolus injection (1). Other effects of IGF I are the growth-promoting actions which have been documented in several metabolic conditions which have low IGF I levels in common, e.g. hypophysectomized rats (2), diabetic rats (3) and Snell dwarf mice (4). Further, prolonged subcutaneous infusions of IGF I to hypophysectomized rats (5) led to a significant weight gain of the kidneys. Similar findings were reported in Snell dwarf mice (4). In all these studies there was no indication of any improvement of kidney function by IGF I. In particular there exists no report on the improvement of glomerular filtration and renal plasma flow during administration of IGF I.